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Recently, several reports demonstrated functional expression of calcium-sensing receptor (CaSR) in the heart. Initial reports found the CaSR to be present in the cardiomyocytes, in contrast a recent report have found the CaSR to be present in sheep fibroblasts of the heart. The calcimimetic drug AMG 073 is a pharmacological (allosteric) modulator of CaSR that is in clinical use for the treatment of hyperparathyroidism. Here, we show that CaSR mRNA levels were up- regulated in the hearts from rats having myocardial infarction (MI) compared to sham operated rats. Furthermore, we found that in rat cardiomyocytes AMG 073 in the presence of extracellular Ca 2+ decreased mRNA levels of atrial natriuretic pre-pro peptide (pre-pro-ANP), which is a marker for cardiac hypertrophy. Surprisingly, CaSR mRNA was not detectable in rat neonatal ventricular fibroblasts (RNVF) by reverse transcriptase PCR. Yet, extracellular calcium exerts a biphasic response in DNA synthesis of RNVFs and AMG 073 seems to suppress DNA synthesis in RNVFs. In addition, calcium and calcimimetic activate MEK/ERK signalling in RNVFs that appears to be independent of CaSR activation. From these results it appears that an additional calcium-sensing mechanism may exist in RNVF. Our findings may be of importance in regards to a potential protective role of calcium and perhaps CaSR against cardiac hypertrophy.

the open endocrinology journal

The Calcium-Sensing Receptor is Upregulated in Post Myocardial Infarct Hearts and Downregulates ANP Expression in Rat Cardiac Myocytes but is Not Expressed in Rat Cardiac Fibroblasts In Vitro